Vomiting and Malabsorption in Children Flashcards

1
Q

Types of vomiting

A

Vomiting with retching
Projectile vomiting
Bilious vomiting
Effortless vomiting

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2
Q

Phases and features of these phases of vomiting with retching

A

Pre-ejection phase

  • pallor
  • nausea
  • tachycardia

Ejection phase

  • retch
  • vomit

Post-ejection phase

  • weakness, pale and limp
  • shivering
  • lethargy
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3
Q

What stimulates vomiting centre?

A
enteric pathogens 
Intestinal inflammation 
Metabolic derangement 
Infection 
Head injury 
Visual stimuli 
Middle ear stimuli
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4
Q

Features of bilious vomiting

A

Should always ring alarm bells

Due to intestinal obstruction until proven otherwise

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5
Q

Causes of bilious vomiting

A
Intestinal atresia 
Malrotation +/- volvulus 
Intussusception 
Ileus 
Crohn's disease with strictures
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6
Q

Investigations of bilious vomiting

A

Abdominal x-ray
Consider contrast meal
Surgical opinion re exploratory laparotomy

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7
Q

Daily, how much fluid enters the duodenum, and how much of this gets to the colon and is lost in faeces?

A

9L enters duodenum each day
1.5L gets to colon
< 200ml lost in faeces

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8
Q

What causes the 600-fold increase in surface area of the small intestine?

A

Mucosal folds

Villi

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9
Q

Essential secretory component of GI tract

A

Water for fluidity/enzyme transport/absorption
Ions
Defence mechanism against pathogens

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10
Q

Features of pyloric stenosis

A
Babies
4-12 weeks old
Boys > girls 
Projectile non-bilious vomiting 
Weight loss
Dehydration +/- shock
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11
Q

Characteristic electrolyte disturbance in pyloric stenosis

A

Metabolic acidosis
Hypocholoraemia
Hypokalaemia

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12
Q

Features of gastro-oesophageal reflux

A

Movement of gastric contents into the oesophagus - GORD occurs when this causes inflammation
Effortless vomiting
Very common problem in infants
Usually self-limiting and resolves spontaneously

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13
Q

Presenting symptoms of gastro-oesophageal reflux/GORD

A

Gi

  • vomiting
  • haematemesis

Nutritional

  • feeding problems
  • failure to thrive

Respiratory

  • apnoea
  • cough
  • wheeze
  • chest infections

Neurological
- Sandifer’s syndrome

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14
Q

What is Sandifer’s syndrome?

A

Association of GORD with spastic torticollis and dystonic body movements
Nodding and rotation of the head, neck extension, gurgling sounds, writhing movements of limbs and severe hypotonia have been reported
Causal relation between GORD and neurological manifestations of Sandifer’s syndrome is supported by the resolution of the manifestations on successful treatment of GORD

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15
Q

Medical assessment of GORD

A

History and examination often sufficient
Radiological investigations
- Video fluoroscopy (only if swallowing problems)
- Barium swallow

pH study - gold standard
Oesophageal impedance monitoring
Endoscopy if not resolved in 2 years or severe symptoms

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16
Q

What features or GORD can be picked up on radiology?

A

Dysmotility
Reflux
Gastric emptying
Strictures

17
Q

Treatment of gastro-oesophageal reflux

A

Feeding advice
Nutritional support
Medical treatment
Surgery

18
Q

Feeding advice for gastro-oesophageal reflux

A

Feed thickeners e.g. carobel
Appropriateness of foods - texture and amount
Behavioural programme - oral stimulation, removal of aversive stimuli
Feeding position - 45 degrees

19
Q

Nutritional support for gastro-oesophageal reflux

A

Calorie supplements
Exclusion diet
Nasogastric tube
Gastrotomy

20
Q

Medical treatment of gastro-oesophageal reflux

A

Feed thickener e.g. gaviscon
Prokinetic drugs
Acid-suppressing drugs

21
Q

Indications for surgery for gastro-oesophageal reflux

A

Failure of medical treatment

Persistent

  • failure to thrive
  • aspiration
  • oesophagitis

Vomiting without complications is not an indication

22
Q

Features of Nissen Fundoplication

A

Children with cerebral palsy are more likely to have complications of bloat, dumping and retching after surgery
Successful surgery may unmask more generalised GI motility problems in the child
Post-operative course may be more complicated in children with cerebral palsy

23
Q

Chronic diarrhoea definition

A

4 or more stools per week

  • < 1 week = acute diarrhoea
  • 2-4 weeks = persistent diarrhoea
  • > 4 weeks = chronic diarrhoea
24
Q

Causes of chronic diarrhoea

A

Motility disturbance

  • toddler’s diarrhoea
  • irritable bowel syndrome

Active secretion

  • acute infective diarrhoea
  • IBD
  • secretory

Malabsorption of nutrients

  • food allergy
  • CF
  • coeliac disease
  • osmotic
25
Q

Features of osmotic diarrhoea

A

Movement of water into the bowel to equilibrate osmotic gradient
Usually a feature of malabsorption - enzymatic defect or transport defect
Mechanism of action of lactulose/movicol
Generally accompanied by macroscopic and microscopic intestinal injury
Clinical remission with removal of causative agent

26
Q

Types of carbohydrate malabsorption

A
Primary lactose malabsorption very rare
Secondary lactose malabsorption e.g. rotavirus infection 
Glucose-galactose malabsorption 
Fructose malabsorption 
Disaccharidases deficiency
27
Q

Causes of fat malabsorption

A

Pancreatic Disease

  • Diarrhoea due to lack of lipase and resultant steatorrhoea
  • Classically cystic fibrosis

Hepatobiliary Disease

  • Chronic liver disease
  • Cholestasis
28
Q

Features of secretory diarrhoea

A

Classically associated with toxin production from vibrio cholerae and enterotoxigenic E. coli - in cholera, can lose 24L per day
Intestinal fluid secretion predominantly driven by active Cl- secretion via CFTR

29
Q

Features of motility diarrhoea

A

Classically toddler’s diarrhoea

Other causes - irritable bowel syndrome, congenital hyperthyroidism, chronic intestinal pseudo-obstruction

30
Q

Features of inflammatory diarrhoea

A

Mixed bag
Malabsorption due to intestinal damage
Secretory effect of cytokines
Accelerated transit time in response to inflammation
Protein exudate across inflamed epithelium

31
Q

Important features of history of a child with diarrhoea

A
Age at onset 
Abrupt/gradual onset
Family history 
Nocturnal defaecation - suggests organic pathology 
Consider growth and weight gain of child
32
Q

Components of faeces analysis

A

Appearance
Stool culture
Determination of secretory vs osmotic

33
Q

What percentage of Western population are affected by coeliac disease?

A

1%

34
Q

Presentation of coeliac disease

A
Abdominal bloating 
Diarrhoea 
Failure to thrive
Short stature
Constipation 
Tiredness
Dermatitis herpatiformis
35
Q

Susceptible asymptomatic group to coeliac disease

A

Type 1 DM
Autoimmune thyroid disease
Down syndrome
First degree relatives of people with coeliac disease

36
Q

Screening tests for coeliac disease

A

Serological screens

  • anti-tissue transglutaminase
  • anti-endomysial
  • concurrent IgA deficiency in 2% may result in false negatives

Gold standard - duodenal biopsy

Genetic testing - HLA DQ2, DQ8

37
Q

ESPCHAN/BSPCHAN Guidelines for coeliac disease

A
Symptomatic children 
Anti-TTG > 10 times upper limit of normal 
Positive anti-endomysial antibodies 
Normal serum IgA 
HLA DQ2, DQ8 positive 
Diagnose coeliac disease without biopsy
38
Q

Treatment of coeliac disease

A

Strict gluten-free diet for life - avoid rye, wheat and barley

Gluten must not be removed prior to diagnosis as serological and histological features will resolve

In very young (< 2 years) re-challenge and re-biopsy may be warranted

Increased risk of rare small bowel lymphoma if untreated